Objectives are to (1) relate ECG distributions to local cardiac excitation and recovery with the specific purpose of predicting ventricular fibrillation, (2) improve definition of factors affecting vulnerability to fibrillation. Methods are computer simulation of fibrillation and animal experimentation. The simulation includes disparate cycle length dependent refractoriness, slow propagation during incomplete recovery, conduction defects, fibrillation threshold and ECG maps. Experiments include body and cardiac surface ECG maps, fibrillation threshold and interventions affecting the vulnerability. Rationale is (1) local nonuniform excitation and recovery are determinants of both vulnerability and ECG distribution features, (2) simulation will show relations pertinent to ECG prediction of fibrillation and improved definition of vulnerability (3) the presence of similar relations can be determined in the heart and (4) detailed mechanisms of the relations can be determined in the simulation and be useful hypotheses for future tests in the heart. Three projects are proposed with the specific goals of (1) identification of ECG markers of vulnerability (2) determining effects of lesion size and geometry on vulnerability and (3) confirming and extending preliminary evidence of a complex relation between induction of fibrillation and severity of initiating agency namely gaps as severity of the initiating agency is increased. Studies are expected to contribute to the medically important goals of predicting fibrillation from the ECG and elucidation of factors affecting vulnerability including effects of lesion size and geometry. Findings concerning severity of initiating agency are expected to elucidate reasons for variability in occurrence of fibrillation including its onset with minor degrees of disease. Important items in feasibility of the research are (1) choice of a 2- dimensional computer model suitable for the large number of simulations proposed and (2) the plan to correlate model and experimental findings in terms of similar phenomena such as gaps but not detailed fibrillation mechanisms.